ArticleAging2022
Ischemic postconditioning protects nonculprit coronary arteries against ischemia-reperfusion injury via downregulating miR-92a, miR-328 and miR-494.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Microtubule dynamics and post-translational modifications in cardiovascular diseases: mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2026Review
- A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats.Reviews in cardiovascular medicine · 2024Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNonculprit lesions are closely related to the prognosis of patients with ST-segment elevation myocardial infarction (STEMI). Our previous research found that ischemic postconditioning (IP) could inhibit the progression of nonculprit lesions. However, the mechanism by which IP regulates the occurrence and development of nonculprit lesions remains unclear.
methodsFirstly, a rabbit ischemia-reperfusion (IR) model was constructed. Next, the morphological characteristics of the coronary arterial tissues and myocardial tissues of the rabbits were observed using hematoxylin-eosin (H&E) staining. Then, western blot was performed to detect the expressions of AT1, Cx43, β-tubulin, Bax, Bcl-2 and cleaved caspase 3. Finally, to further confirm the effect of IP on nonculprit coronary arterial tissues, an
resultsIR notably induced the cells apoptosis in nonculprit coronary arterial tissues and in myocardial tissues, while IR-induced cell apoptosis was significantly inhibited by IP. In addition, IP protected nonculprit coronary arterial tissues against IR via downregulating miR-92a, miR-328 and miR-494 and mRNA AT1, Cx43 and β-tubulin. Consistently, OGD/R-induced injury of Human umbilical vein endothelial cells (HUVECs) was reversed by IP.
conclusionsIn this study, IP could protect nonculprit coronary arteries against IR injury via downregulating miR-92a, miR-328 and miR-494. Our findings may provide new directions for the treatment of nonculprit lesions.
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Registered trials
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